The beta-adrenergic blocking agents have been in clinical use for almost a decade and are now approved for use in many situations. The beta-adrenergic blocking drug propranolol is particularly effective in the treatment of angina pectoris and has been shown to decrease the number of attacks while increasing exercise tolerance. Propranolol exerts its effect by attenuating the effect of cardiac sympathetic simulation, thus reducing oxygen utilization through diminution of heart rate and ventricular systolic pressure. With the widespread use of propranolol, a number of adverse effects were noted after abrupt discontinuation of the drug in patients with ischemic heart disease. There are many reported instances in the literature where patients developed unstable angina, myocardial infarction, and some died as a result of abrupt propranolol withdrawal. The explanation for this clinical syndrome has been speculative and has been referred to by some as a rebound phenomenon. However, a pharmacological or physiological basis for its existence has not been fully explored. It is the purpose of this investigation to study the effects of chronic propranolol administration on cardiac and adrenal catecholamine levels with special emphasis on the withdrawal state using a small animal model. albino guinea pigs will receive propranolol 5 mg/kg of body weight by subcutaneous injection twice daily. At the end of two weeks the animals will be sacrificed at various times following the last dose of propranolol, and the atria and ventricles will be assayed, for propranolol, norepinephrine and tyrosine hydroxylase activity. The adrenal glands will also be assayed for norepinephrine and tyrosine hydroxylase, the rate-limiting enzyme in the catecholamine biosynthetic pathway. Information gathered from this study will better define the relationship between the beta-blocking agents and tissue catecholamines and perphaps will lead to a better understainding of the syndrome of abrupt propranolol withdrawal.